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Chipashvili O, Utter DR, Bedree JK, et al. Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation. Cell Host Microbe. 2021;29(11):1649-1662.e7doi: 10.1016/j.chom.2021.09.009.
Chipashvili, O., Utter, D. R., Bedree, J. K., Ma, Y., Schulte, F., Mascarin, G., Alayyoubi, Y., Chouhan, D., Hardt, M., Bidlack, F., Hasturk, H., He, X., McLean, J. S., & Bor, B. (2021). Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation. Cell host & microbe, 29(11), 1649-1662.e7. https://doi.org/10.1016/j.chom.2021.09.009
Chipashvili, Otari, et al. "Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation." Cell host & microbe vol. 29,11 (2021): 1649-1662.e7. doi: https://doi.org/10.1016/j.chom.2021.09.009
Chipashvili O, Utter DR, Bedree JK, Ma Y, Schulte F, Mascarin G, Alayyoubi Y, Chouhan D, Hardt M, Bidlack F, Hasturk H, He X, McLean JS, Bor B. Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation. Cell Host Microbe. 2021 Nov 10;29(11):1649-1662.e7. doi: 10.1016/j.chom.2021.09.009. Epub 2021 Oct 11. PMID: 34637779; PMCID: PMC8595704.
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Cell Host Microbe. 2021 Nov 10;29(11):1649-1662.e7. doi: 10.1016/j.chom.2021.09.009. Epub 2021 Oct 11.

Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation.

Cell host & microbe

Otari Chipashvili, Daniel R Utter, Joseph K Bedree, Yansong Ma, Fabian Schulte, Gabrielle Mascarin, Yasmin Alayyoubi, Deepak Chouhan, Markus Hardt, Felicitas Bidlack, Hatice Hasturk, Xuesong He, Jeffrey S McLean, Batbileg Bor

Affiliations

  1. The Forsyth Institute, Cambridge, MA 02142, USA.
  2. Division of Geological and Planetary Sciences, California Institute of Technology, Pasadena, CA 91125, USA.
  3. The Forsyth Institute, Cambridge, MA 02142, USA; Section of Oral Biology, Division of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  4. The Forsyth Institute, Cambridge, MA 02142, USA; Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA.
  5. The Forsyth Institute, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
  6. Department of Periodontics, University of Washington, Seattle, WA 98119, USA; Department of Microbiology, University of Washington, Seattle, WA 98195, USA.
  7. The Forsyth Institute, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA. Electronic address: [email protected].

PMID: 34637779 PMCID: PMC8595704 DOI: 10.1016/j.chom.2021.09.009

Abstract

Saccharibacteria (TM7) are obligate epibionts living on the surface of their host bacteria and are strongly correlated with dysbiotic microbiomes during periodontitis and other inflammatory diseases, suggesting they are putative pathogens. However, due to the recalcitrance of TM7 cultivation, causal research to investigate their role in inflammatory diseases is lacking. Here, we isolated multiple TM7 species on their host bacteria from periodontitis patients. These TM7 species reduce inflammation and consequential bone loss by modulating host bacterial pathogenicity in a mouse ligature-induced periodontitis model. Two host bacterial functions involved in collagen binding and utilization of eukaryotic sialic acid are required for inducing bone loss and are altered by TM7 association. This TM7-mediated downregulation of host bacterial pathogenicity is shown for multiple TM7/host bacteria pairs, suggesting that, in contrast to their suspected pathogenic role, TM7 could protect mammalian hosts from inflammatory damage induced by their host bacteria.

Copyright © 2021 Elsevier Inc. All rights reserved.

Keywords: Actinobacteria; Actinomyces; Saccharibacteria; TM7; bacterial symbiosis; candidate phyla radiation; human microbiome; human oral microbiome; inflammatory disease; periodontitis

Conflict of interest statement

Declaration of interests The authors declare no competing interests.

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